Errr, spontaneous mutation?? Selection pressure for such mutations that are still survivable for the bacteria?
I just described a very rough screening method, pcrh quotes from the Nature article other extreme efforts tried. These don't produce specific types of mutations, they just discover if there are any "easy" ones. E.g. the E. Coli antibiotic I mentioned had to be transported across the membrane bacterium by a protein.
The lab I did part of a summer's research was working with the enterobactin iron scavenging mechanism in E. Coli (https://en.wikipedia.org/wiki/Enterobactin). If grown in seriously iron free condition (e.g. glassware was soaked in HCl, and then bathed in deionized water for days), it would synthesize iron binding enterobactin and send it out into the environment, and there was a protein on the membrane surface that would accept the enterobactin+iron complex.
This also turned out to be the protein that accepted this antibiotic into E. Coli. It appeared that some of the mutations that allowed this were either point or deletion mutations of that protein, either it was deranged or cut off in some location, or outright deleted (missing from the bacteria's set of genes in its DNA).
So this survival mechanism is one of just not letting the antibiotic inside in the first place, which is how it appears teixobactin producing bacteria survive it. They appear to synthesize and expel it, and they don't have cell walls allowing it to get back in.
I just described a very rough screening method, pcrh quotes from the Nature article other extreme efforts tried. These don't produce specific types of mutations, they just discover if there are any "easy" ones. E.g. the E. Coli antibiotic I mentioned had to be transported across the membrane bacterium by a protein.
The lab I did part of a summer's research was working with the enterobactin iron scavenging mechanism in E. Coli (https://en.wikipedia.org/wiki/Enterobactin). If grown in seriously iron free condition (e.g. glassware was soaked in HCl, and then bathed in deionized water for days), it would synthesize iron binding enterobactin and send it out into the environment, and there was a protein on the membrane surface that would accept the enterobactin+iron complex.
This also turned out to be the protein that accepted this antibiotic into E. Coli. It appeared that some of the mutations that allowed this were either point or deletion mutations of that protein, either it was deranged or cut off in some location, or outright deleted (missing from the bacteria's set of genes in its DNA).
So this survival mechanism is one of just not letting the antibiotic inside in the first place, which is how it appears teixobactin producing bacteria survive it. They appear to synthesize and expel it, and they don't have cell walls allowing it to get back in.